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Vacuolar Hepatopathy



BASIC INFORMATION image



DEFINITION


Benign, reversible hepatic lesion of glycogen accumulation that occurs commonly in dogs in response to excess glucocorticoids and/or as a reactive change secondary to systemic disorders



SYNONYMS


Glucocorticoid hepatopathy, hepatic glycogen accumulation, steroid hepatopathy



EPIDEMIOLOGY


SPECIES, AGE, SEX: Dogs only; age and sex dependent on underlying cause. Older dogs may have spontaneous hyperadrenocorticism or idiopathic vacuolar hepatopathy.



GENETICS & BREED PREDISPOSITION



• Poodles, dachshunds, beagles, boxers, terrier breeds: pituitary-dependent hyperadrenocorticism

• German shepherd, Labrador retriever, poodle, dachshund, terrier breeds: functional adrenal tumor

• Scottish terriers: idiopathic vacuolar hepatopathy

RISK FACTORS: Glucocorticoid administration


ASSOCIATED CONDITIONS & DISORDERS: Hyperadrenocorticism including atypical forms (increased adrenal steroids other than cortisol, or abenant adrenocortical disease [see p. 6]); secondary reactive change associated with stress from other systemic inflammatory, infectious, or neoplastic disorders.



CLINICAL PRESENTATION



DISEASE FORMS/SUBTYPES



• Incidental finding of increased serum alkaline phosphatase (ALP) activity; subsequent fine-needle aspirate (FNA) and Cytologic examination or liver biopsy show vacuolar change

• Clinical signs of glucocorticoid excess

• Clinical signs of primary systemic disorder


HISTORY, CHIEF COMPLAINT



• For glucocorticoid excess, clinical signs reflect systemic effects of hyper-cortisolism rather than hepatic disease: polyuria and polydipsia (PLJ/PD), polyphagia, panting.

• If iatrogenic, a history of glucocorticoid administration (oral, injectable, topical: eyes, ears, skin) within last 3-6 months (depends on route, preparation, duration of therapy, and individual sensitivity) is expected.

• Other signs depend on primary systemic disorder.

• The patient may show no clinical signs (incidental finding) or mild polydipsia: idiopathic vacuolar hepatopathy, Scottish terriers.


PHYSICAL EXAM FINDINGS



• For iatrogenic or spontaneous hyperadrenocorticism: hepatomegaly (may be massive); abdominal enlargement, thin haircoat or truncal alopecia, thin skin

• Other findings dependent on primary systemic disorder

• May be unremarkable


ETIOLOGY AND PATHOPHYSIOLOGY



• Excess glucocorticoids (exogenous, or spontaneous hyperadrenocorticism):
○ Dogs are uniquely susceptible to hepatic effects of glucocorticoids.

○ Gradual hepatic glycogen accumulation and hepatomegaly occur within the first 2 weeks of daily prednisolone administration.

○ Preceded by increased serum ALP activity

○ Marked individual variation

○ Lesions identical with exogenous or endogenous corticosteroids

○ Hepatic function is typically normal.

○ Reversible

• Aberrant adrenocortical disease (“atypical hyperadrenocorticism;” see p. 6)
○ Increased adrenal steroid hormones other than cortisol (especially progesterone and 17-α hydroxyprogesterone)

○ Progesterone has glucocorticoid-like effects on the liver.

• Scottish terriers:
○ Increased serum ALP activity (predominantly steroid-induced isoenzyme)

○ No overt clinical signs; cause unknown

○ No association between progesterone or 17-α hydroxyprogesterone levels and serum ALP elevations

• Reactive hepatopathy:

○ Common lesion in dogs with other systemic illnesses (including neoplastic, neurologic, immune-mediated, and gastrointestinal tract disorders) and severe dental disease.

○ Acute or chronic illness can be associated with stress-induced hypercortisolemia resulting in vacuolar hepatopathy.

• Hepatic nodular hyperplasia or regeneration:
○ Etiology unknown; may be associated with nutritional factors or the result of focal areas of ischemia

• Congenital or acquired hepatobiliary disease:
○ Acute and chronic inflammation, hepatotoxicity, and congenital portosystemic shunt may have vacuolar changes. With acquired hepatobiliary disease, necrotic or inflammatory lesions predominate.

• Idiopathic vacuolar hepatopathy:
○ Excess corticosteroids or other adrenal steroid hormones cannot be documented; absence of systemic disease; usually associated with no clinical signs; clinical significance unknown.


DIAGNOSIS image



DIAGNOSTIC OVERVIEW



• Initially suspected based on findings of increased serum ALP activity (steroid-induced isoenzyme predominates), normal liver function, and hepatomegaly.

• Abdominal ultrasound to evaluate for other causes of liver disease and to evaluate adrenal glands; FNA cytologic examination of liver shows characteristic vacuoles (though common false-positive finding with FNA).

• Screen for excess exogenous or endogenous glucocorticoids (endocrine testing for hyperadrenocorticism if compatible with history and physical exam), then evaluate for systemic disorders causing reactive change; if no diagnosis, consider liver biopsy to evaluate for primary hepatobiliary disorders.


DIFFERENTIAL DIAGNOSIS



• Other hepatopathies (inflammatory, neoplastic)

• Nodular hyperplasia or regeneration

• Hyperlipidemia:
○ Diabetes mellitus

○ Hypothyroidism

○ Familial in miniature schnauzers, Shetland sheepdogs, others

• Superficial necrolytic dermatitis (hepatocutaneous syndrome)

• Exocrine pancreatic insufficiency

• Chronic pancreatitis

• Tetracycline administration

• Glycogen or lysosomal storage disease


INITIAL DATABASE



• CBC: lymphopenia, eosinopenia (excess glucocorticoids), other abnormalities depending on primary systemic disorder

• Serum biochemistry panel: serum ALP activity increased, may be marked, predominantly due to steroid-induced isoenzyme of ALP. Serum alanine aminotransferase (ALT) activity shows mild to moderate increases (or levels may be normal). Increased serum cholesterol concentration (excess glucocorticoids). Other biochemistry values typically normal (bilirubin, albumin).

• Serum bile acids concentration normal to mildly increased

• Abdominal radiographs: hepatomegaly (may be marked)

• Abdominal ultrasound: diffusely hyperechoic liver; may also be mottled and/or nodular; adrenomegaly (hyperadrenocorticism)


ADVANCED OR CONFIRMATORY TESTING



• FNA and cytologic evaluation of liver:
○ Ballooned hepatocytes with decreased cytoplasmic density, commonly described as vacuolar hepatopathy

○ Vacuolar hepatopathy is a common false-positive finding with FNA

• Liver biopsy and histopathologic evaluation:
○ Patchy distribution of ballooned hepatocytes with decreased cytoplasmic density. Glycogen accumulation is characteristic. Glycogen accumulation can be differentiated from hydropic degeneration with periodic acid-Schiff (PAS) stains for glycogen; oil red O (ORO) stain to differentiate lipid vacuoles

○ No evidence of inflammation, necrosis, or cholestasis

• Rule out spontaneous hyperadrenocorticism:
○ Review clinical history and physical exam

○ Low-dose dexamethasone suppression test or adrenocorticotropic hormone (ACTH) stimulation test to screen for hyperadrenocorticism

○ Endogenous ACTH level, high-dose dexamethasone suppression test, and adrenal gland ultrasonography to differentiate pituitary from adrenal causes

○ Adrenal steroid profile before and after ACTH to diagnose aberrant adrenocortical disease

• Evaluate for other systemic disorders that could cause secondary reactive vacuolar hepatopathy.


TREATMENT image



TREATMENT OVERVIEW


Focus therapeutic efforts on treating underlying disorder.



CHRONIC TREATMENT



• If the patient is receiving high doses of glucocorticoids and is showing clinical signs of hepatic disease (e.g., lethargy or depression, difficult to distinguish from underlying condition), other immunosuppressive drugs such as azathioprine or cyclosporine may be warranted to allow dose reduction of glucocorticoids.

• Idiopathic vacuolar hepatopathy:
○ If no clinical signs are present, treatment may not be warranted.

○ Necessity or clinical effectiveness of hepatoprotective drug therapy (S-adenosylmethionine, vitamin E) unknown.


POSSIBLE COMPLICATIONS



• Hyperadrenocorticism (see p. 548) and complications involving glucocorticoid excess

• Severe vacuolar hepatopathy has been associated with development of gallbladder mucocele.


RECOMMENDED MONITORING


Idiopathic vacuolar hepatopathy: because some dogs may eventually develop spontaneous hyperadrenocorticism, monitor for clinical signs and follow up with screening tests (low-dose dexamethasone suppression test or ACTH stimulation) as needed.



PROGNOSIS AND OUTCOME image



• Idiopathic vacuolar hepatopathy; vacuolar hepatopathy of Scottish terriers:
○ Benign clinical course

○ Good long-term prognosis

○ Some dogs may eventually develop clinical hyperadrenocorticism

• Exogenous glucocorticoid therapy:
○ Vacuolar hepatopathy is reversible once glucocorticoids are discontinued; may require weeks to months.


PEARLS & CONSIDERATIONS image



COMMENTS



• Diagnostic and therapeutic efforts should be directed at identifying and correcting causes of glucocorticoid excess or primary systemic disorders.

• Hepatic function is typically preserved. If serum ALT > ALP or if hypoalbuminemia, hyperbilirubinemia, or markedly increased serum bile acids concentration are present, a more serious primary hepatobiliary disorder may be present and should be identified and treated. In rare instances, severe vacuolar hepatopathy has been associated with overt hepatic dysfunction, which may be fatal.

• Presence of increased serum ALP activity and vacuolar hepatopathy does not preclude continued use of corticosteroids if their administration is necessary. Liver function is generally preserved; benign lesion. Whenever possible, make an attempt to minimize systemic effects of glucocorticoids with alternate-day therapy using lowest effective dose possible (prednisolone or prednisone), and/or use other immunosuppressive drugs (azathioprine, cyclosporine).

• Cats that are receiving glucocorticoids (or with hyperadrenocorticism) rarely develop vacuolar hepatopathy.


PREVENTION


If long-term glucocorticoid therapy is necessary, give oral prednisolone or prednisone (rather than oral dexamethasone or injectable long-acting forms) at the lowest dose possible on alternate days to minimize the systemic (including hepatic) effects of glucocorticoids. Also consider administering other immunosuppressive drugs (e.g., azathioprine, cyclosporine) to allow dose reduction of glucocorticoids.



CLIENT EDUCATION


Idiopathic vacuolar hepatopathy appears to be clinically benign.



SUGGESTED READING



Gary AT, Webb CB, Twedt DC: Investigation of idiopathic vacuolar hepatopathy in Scottish terriers and the role of progesterone steroids in the etiology. Proceedings of the American College of Veterinary Internal Medicine forum, Louisville, KY, May 31-June 3, 2006.


Sepesy LM, Center SA, Randolph JF, et al. Vacuolar hepatopathy in dogs: 336 cases (1993-2005). J Am Vet Med Assoc. 2006;229:246.



Vaginal Congenital Abnormalities in the Bitch



AUTHOR: SUSAN E. JOHNSON



EDITOR: KEITH P. RICHTER



BASIC INFORMATION image



DEFINITION


Malformations that reduce the diameter of the vestibulovaginal junction (bands) and may cause secondary infertility, vaginitis, or cystitis include incomplete dissolution or fusion of the paramesonephric ducts (Müllerian), hymenal remnants, and hypoplasia of the vestibulovaginal junction.



EPIDEMIOLOGY


SPECIES, AGE, SEX: Congenital vaginal abnormalities are present at birth but are usually undetected until the appearance of clinical signs. Young-adult female dogs are most commonly affected.


GENETICS & BREED PREDISPOSITION: Large-breed dogs may be over-represented.


ASSOCIATED CONDITIONS & DISORDERS: Female dogs with ectopic ureters often have coincident congenital vaginal abnormalities.



CLINICAL PRESENTATION



DISEASE FORMS/SUBTYPES



• Double vagina

• Hypoplasia of the vaginal vault

• Imperforate hymen

• Vaginal stenosis

• Vaginal stricture


HISTORY, CHIEF COMPLAINT



• Unsuccessful breeding attempts, obvious pain during breeding, avoidance of male during breeding attempts

• Purulent, often recurrent vaginal discharge

• Persistent urinary tract infection (UTI), urine dribbling


PHYSICAL EXAM FINDINGS



• Vaginal discharge may be present.

• Narrowing of vestibulovaginal junction may be apparent during manual vaginal exam (see p. 1360).


ETIOLOGY AND PATHOPHYSIOLOGY



• Incomplete fusion of the paramesonephric ducts can result in persistent dorsoventral bands.

• Vestibulovaginal hypoplasia causes concentric narrowing of the vestibulovaginal junction.

• Incomplete dissolution of the hymen can compromise the vestibulovaginal junction.

• Any type of vestibulovaginal stricture can interfere with breeding, owing to pain produced during penetration by a male dog.

• Anatomic abnormalities of the vestibulovaginal junction can inhibit drainage of vaginal secretions, which can lead to vaginitis or ascending UTI.


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


Clinicians should suspect vestibulovaginal abnormalities in bitches or queens with a history of difficult or unsuccessful breeding. The diagnosis is usually made during vaginal examination.



DIFFERENTIAL DIAGNOSIS



• Behavioral abnormalities in breeding bitches in estrus who are reluctant to stand for a male

• Urolithiasis is a much more common cause of chronic UTI.

• Vaginal discharge may be associated with juvenile-onset vaginitis or pyometra.


INITIAL DATABASE



• Vaginoscopy using a flexible or rigid endoscope (see p. 1361)

• Heavy sedation or general anesthesia is necessary.


ADVANCED OR CONFIRMATORY TESTING


Contrast radiography: retrograde vaginography (see p. 1158)



TREATMENT image



TREATMENT OVERVIEW


Remove obstruction/narrowing at vestibulovaginal junction.



ACUTE GENERAL TREATMENT



• Digital dilation of vestibulovaginal junction (effective for treatment of hymenal remnants or mild [membranous] vestibulovaginal stenosis)

• Resection of dorsoventral paramesonephric duct remnants or bands if present

• For severe (fibrous) vestibulovaginal stenosis: resection and anastomosis of vestibulovaginal junction via an extended episiotomy


CHRONIC TREATMENT


After manual or surgical dilation, antibiotic therapy (based on culture and sensitivity [C&S]) may have to be extended up to 6 weeks for treatment of ascending UTI if present.



BEHAVIOR/EXERCISE


Bitches with previous painful breeding episodes may be reluctant to accept a male after treatment of vestibulovaginal abnormalities. Use of an experienced breeding male may be helpful.



POSSIBLE COMPLICATIONS



• Stricture secondary to resection and anastomosis

• Inadequate resection does not resolve clinical signs.


RECOMMENDED MONITORING


Observe the animal for recurrence of signs; initial treatment may have to be repeated if stricture occurs secondary to resection or traumatic dilation.



PROGNOSIS AND OUTCOME image



• Prognosis is good if clinical signs are caused by hymenal remnants or mild vaginal stricture.

• Prognosis for resolution of clinical signs is fair to good for severe vaginal stricture treated by vestibulovaginal resection and anastomosis.


PEARLS & CONSIDERATIONS image



COMMENTS



• Do not confuse normal narrowing at the vestibulovaginal junction with a pathologic condition:
○ The diameter of the vestibulovaginal junction must be less than 30% of the diameter of the maximal diameter of the vagina to be considered pathologic.

• Most congenital vaginal abnormalities do not cause clinical signs.


PREVENTION


Since most vestibulovaginal abnormalities are congenital but not hereditary, there are no recommendations against breeding affected bitches or queens once the abnormality is treated.



TECHNICIAN TIPS


Although digital vaginal examination is helpful in making a diagnosis of vestibulovaginal abnormality, direct visual inspection using vaginoscopy permits a much more accurate diagnosis.



CLIENT EDUCATION



• Breeding bitches that are reluctant to stand for a male may have vestibulovaginal abnormalities that cause painful breeding.

• Congenital vaginal anomalies may be present without causing clinical signs.


SUGGESTED READING



Crawford JT, Adams WM. Influence of vestibulovaginal stenosis, pelvic bladder, and recessed vulva on response to treatment for clinical signs of lower urinary tract disease in dogs: 38 cases (1990-1999). J Am Vet Med Assoc. 2002;221:995.


Kyles AE, et al. Vestibulovaginal stenosis in dogs: 18 cases (1987-1995). 1 Am Vet Med Assoc. 1996;209:1889.



Vaginal Hyperplasia and Vaginal Prolapse



AUTHOR: JAMES A. FLANDERS



EDITOR: MICHELLE A. KUTZLER



BASIC INFORMATION image



DEFINITION


Edematous swelling of the vaginal mucosa cranial to the urethral orifice; an uncommon disorder that occurs during estrogen stimulation in the intact bitch. It may progress to vaginal protrusion through the vulvar lips.



SYNONYMS


Vaginal edema, hypertrophy, hyperplasia, eversion, or protrusion



EPIDEMIOLOGY


SPECIES, AGE, SEX: Intact bitch, any age (7 months to 16 years old)



GENETICS & BREED PREDISPOSITION



• More common in large-breed dogs

• Breeds predisposed: bulldog, mastiff, boxer, dalmatian, German shepherd, Saint Bernard, Labrador and Chesapeake Bay retrievers, weimaraner, Walker hound, springer spaniel, Airedale terrier, and American pit bull terrier


RISK FACTORS



• Young bitch under the influence of estrogen during proestrus or estrus; may occur or recur during diestras, pregnancy, or parturition

• Can be observed as side effect of estrus induction with estrogen

ASSOCIATED CONDITIONS & DISORDERS: Markedly prolapsed vaginal tissue is subject to self-mutilation and may be dry, ulcerated, necrotic, and devascularized; possible dysuria or pollakiuria.



CLINICAL PRESENTATION



DISEASE FORMS/SUBTYPES


Vaginal hyperplasia:


• Type I: slight to moderate eversion of the vaginal floor cranial to the urethral orifice; confined to the vestibulum, appearing as a bulge at the perineum.

• Type II: well-developed swelling of the vaginal floor, which may include the lateral vaginal walls, protruding through the vulvar lips. The swelling appears dome shaped.


image VAGINAL HYPERPLASIA AND VAGINAL PROLAPSE A, Well-developed swelling of vaginal floor, which may include lateral vaginal walls, protruding through vulvar lips. Swelling appears dome-shaped (type II vaginal hyperplasia). B, Well-developed protrusion of entire circumference of vaginal wall through vulvar lips. Swelling appears doughnut shaped (vaginal prolapse).

• Type III: well-developed protrusion of the entire circumference of the vaginal wall through the vulvar lips. The swelling appears doughnut shaped and is a vaginal prolapse.


HISTORY, CHIEF COMPLAINT



• Previous occurrence of vaginal hyperplasia

• Onset of proestrus or estrus

• Licking or irritation of the vulva

• Mass protruding from vulva or bulge at the perineum

• Dysuria or pollakiuria

• Failure to allow intromission during breeding

• Tenesmus

PHYSICAL EXAM FINDINGS: Bulge at the perineum or protrusion of a pink dome-shaped or doughnut-shaped mass from vulva; surface of protrusion may be dry, necrotic, or ulcerated. Vaginal examination reveals:


• A urethral orifice located ventrally in all three types of vaginal hyperplasia
○ A vaginal lumen located dorsally in types I and II but centrally located in type III

• By contrast, uterine prolapse is distinguished by the presence of tubular masses within the vagina or protruding from the vulva.


ETIOLOGY AND PATHOPHYSIOLOGY



• Vaginal hyperplasia: an exaggerated response of the vaginal mucosa to estrogen (hyperemia, edema, keratinization). The swelling begins as an eversion in the vaginal floor, cranial to the urethral orifice.

• With vaginal prolapse: histopathologic examination of affected vaginal tissue is consistent with submucosal edema rather than with hyperplasia or hypertrophy.


DIAGNOSIS image



DIAGNOSTIC OVERVIEW


The diagnosis is suspected based on the presence of a vulvar swelling or protrusion in a young intact bitch.



DIFFERENTIAL DIAGNOSIS



• Benign or malignant vaginal neoplasia

• Vaginal polyp

• True vaginal prolapse with concurrent entrapment of visceral organs (rare)

• Uterine prolapse

• Urethral neoplasia


INITIAL DATABASE



• Stage of hormonal cycle based on vaginal cytologic examination

• Vaginal examination to locate the urethral orifice, vaginal lumen, origin of the protruding mass, and the size of its base (see p. 1360)

• Ensure that the animal is able to urinate.


ADVANCED OR CONFIRMATORY TESTING



• Biopsy of vaginal mass confirms diagnosis in atypical bitches.

• In severe cases, survey radiographs can be used to evaluate for visceral organ involvement; contrast radiography can confirm the location of the urethral orifice and vaginal lumen.


TREATMENT image



TREATMENT OVERVIEW


Treatment goals are to prevent drying, necrosis, and devitalization of exposed vaginal tissue, prevent future recurrence, and prevent urethral obstruction.



ACUTE GENERAL TREATMENT



• Insertion of a urethral catheter to relieve obstruction when present
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